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peroxidase/infart
L'enllaç es desa al porta-retalls
Pàgina 1 des de 649 resultats
Selenium levels and glutathione peroxidase activities in patients with acute myocardial infarction.
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OBJECTIVE
Selenium (Se) is part of the enzyme glutathione peroxidase (GSH-Px) that plays an important role in the antioxidant defence of the body, including the myocardium, against the deleterious actions of free radicals and lipid peroxides. In order to evaluate the Se status and the GSH-Px
Effect of acute myocardial infarction on erythrocytic glutathione peroxidase 1 activity and plasma vitamin e levels.
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Glutathione peroxidase 1 (GPX-1) has an important role in antioxidant defense and has been suggested to have a protective role against the pathogenesis of atherosclerosis. In the present study, erythrocytic GPX-1 activity from 42 patients with acute myocardial infarction and 285 healthy control
[Effect of a highly dispersed copper powder on superoxide dismutase and glutathione peroxidase activities in experimental myocardial infarct].
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Administration of highly dispersed copper powder in a dose 0.2 mg/kg three days before modelled coronary-occlusion myocardial infarction caused transitory increase in activity of antioxidant enzymes--superoxide dismutase and glutathione peroxidase in the necrotic zone of myocardium of rats, and also
Increased plasma glutathione peroxidase activity in patients with acute myocardial infarction.
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BACKGROUND
Aim of the study was to determine the concentration of selenium (Se) and the activity of glutathione peroxidase (GSH-Px) in patients with acute myocardial infarction (AMI) and to observe the behavior of these parameters during thrombolysis therapy.
METHODS
The study comprised two groups
Levels of glutathione reductase and glutathione peroxidase of human platelets in unstable angina and myocardial infarction.
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Levels of glutathione peroxidase and glutathione reductase were measured in the platelets of 30 patients, 10 of them affected by unstable angina, 10 of them reperfused after myocardial infarction and 10 matched healthy controls. The specific activities of both the enzymes were lowered in both group
Selenium and myocardial infarction: glutathione peroxidase in platelets.
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The activity of the selenoenzyme glutathione peroxidase (EC 1.11.1.9) was determined in platelets of 15 patients with acute myocardial infarction and 13 control subjects. The platelets of the patients had significantly lower activities of the enzyme (P(t) greater than 0.99). This may be related to
Comprehensive peroxidase-based hematologic profiling for the prediction of 1-year myocardial infarction and death.
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BACKGROUND
Recognition of biological patterns holds promise for improved identification of patients at risk for myocardial infarction (MI) and death. We hypothesized that identifying high- and low-risk patterns from a broad spectrum of hematologic phenotypic data related to leukocyte peroxidase-,
Antioxidant vitamin levels and glutathione peroxidase activity during ischemia/reperfusion in myocardial infarction.
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The consequences of increased oxidative stress, measured as the level of malondialdehyde (MDA) during ischemia/reperfusion, were studied in 48 patients in the acute phase of myocardial infarction (AMI) and a control group (21 blood donors). The serum levels of alpha-tocopherol and beta-carotene were
[Production of oxygen free radicals in myocardial infarction treated by thrombolysis. Analysis of glutathione peroxidase, superoxide dismutase and malondialdehyde].
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Many enzyme systems such as glutathione peroxidase (GPx) or superoxide dismutase (SOD) neutralise the oxygen derived free radicals produced during myocardial reperfusion by thrombolysis. Erythrocytic SOD, plasma and erythrocytic GPx and their cofactor selenium, substances reacting with
Increased infarct size and exacerbated apoptosis in the glutathione peroxidase-1 (Gpx-1) knockout mouse brain in response to ischemia/reperfusion injury.
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Glutathione peroxidase is an antioxidant enzyme that is involved in the control of cellular oxidative state. Recently, unregulated oxidative state has been implicated as detrimental to neural cell viability and involved in both acute and chronic neurodegeneration. In this study we have addressed the
Overexpression of glutathione peroxidase prevents left ventricular remodeling and failure after myocardial infarction in mice.
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BACKGROUND
Oxidative stress plays an important role in the pathophysiology of heart failure. We determined whether the overexpression of glutathione peroxidase (GSHPx) could attenuate left ventricular (LV) remodeling and failure after myocardial infarction (MI).
RESULTS
We created MI in 12- to
Vascular peroxidase 1 is a novel regulator of cardiac fibrosis after myocardial infarction.
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Cardiac fibrosis is the most important mechanism contributing to cardiac remodeling after myocardial infarction (MI). VPO1 is a heme enzyme that uses hydrogen peroxide (H2O2) to produce hypochlorous acid (HOCl). Our previous study has demonstrated that VPO1 regulates myocardial
[Effect of atenolol, dibunol, peroxidase and Astragalus dasynthus on the morphometric parameters of myocardial infarction].
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Experiments were carried out on rats after coronary arterial ligation. In the myocardial infarction region there is the border zone or reversibly damaged zone which may be partially saved from necrosis by using beta-blocking agents. Atenolol, dibunol, Astragalus dasyanthus pall. moderately decrease
Glutathione peroxidase activity in serum during acute myocardial infarction and unstable angina pectoris.
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We studied GSH-Px enzyme activity in serum after acute myocardial infarction (AMI) and unstable angina pectoris (UAP). The study included 15 patients with AMI and 9 patients with UAP. Serum GSH-Px activity in the AMI group (0.992 +/- 0.071) (IU/ml) was higher than that of the UAP group. Serum GSH-Px
Erythrocyte glutathione peroxidase and myocardial infarction.
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